Effects of subarachnoid haemorrhage on intracranial prostaglandins.

Abstract

Prostaglandins E2, F2 alpha, 6 oxo F1 alpha and thromboxane B2 increased in cisternal CSF following mock subarachnoid haemorrhage in dogs, particularly PGE2 (X25.5). Concentrations were increased also in lumbar CSF of five patients some 8 days after subarachnoid haemorrhage. Subarachnoid haemorrhage did not alter the production of prostaglandins by dog whole cortex or choroid plexuses in vitro, but production by pooled dissected cerebral arteries of PGE2 was increased and of 6 oxo F1 alpha was decreased. Intravenous indomethacin decreased prostaglandin production by cerebral tissues, and caused a marked decrease in the prostacyclin metabolite in CSF. The implications of our findings for the aetiology of cerebral vasospasm are discussed.

EP1- and EP3-Receptors Mediate Prostaglandin E2–Induced Constriction of Porcine Large Cerebral Arteries

“…In addition, our present experiments showed that constriction induced by PGE 2 was greatly potentiated by HbO 2 , supporting a potential role for PGE 2 in SAH and suggesting a possible mechanism of interaction between these putative causative agents. This is consistent with the reported role of PGE 2 along with hemoglobin and other eicosanoids in cerebral vasospasm (Chyatte, 1989;Macdonald and Weir, 1991;Pickard et al, 1994;Toda et al, 1991;Walker et al, 1983).…”

“…The interaction between PGE 2 and HbO 2 , both implicated as causative agents in cerebral vasospasm after SAH (Chyatte 1989;Macdonald and Weir, 1991;Pickard et al, 1994;Walker et al, 1983), was examined by studying and comparing PGE 2 -induced constriction before and after incubation with HbO 2 . The PGE 2 -induced constriction in endothelium-denuded porcine basilar arteries in the absence of active muscle tone was potentiated in a concentration-dependent manner after 1-hour incubation with HbO 2 (10 mol/L) (Fig.…”

“…In SAH, prostaglandins and HbO 2 have been invoked as causative agents (Macdonald and Weir, 1991). It has been shown that PGE 2 is the eicosanoid present in the highest concentration in the CSF after SAH (Walker et al, 1983). The levels of PGE 2 in the CSF have been shown to increase 90-fold in dogs (Chyatte, 1989) and up to 250-fold in humans (Pickard et al, 1994) after SAH.…”

“…Prostaglandin E 2 is one of the major mediators produced during certain cerebral vascular dysfunctions, such as the cerebral vasospasm after SAH (Macdonald and Weir, 1991;Toda et al, 1991, Walker et al, 1983 in animals (Chyatte, 1989) and humans (Pickard et al, 1994). Consequently, in SAH, prostaglandins such as PGE 2 and HbO 2 have been invoked as important causative agents (Macdonald and Weir, 1991).…”

Inducible Cyclooxygenase Expression in Canine Basilar Artery After Experimental Subarachnoid Hemorrhage

“…20 Following SAH, levels of arachidonic acid metabolites are elevated in the CNS. 21,22 These prostanoids contribute to the control of cerebrovascular tone and regulation of cerebral blood flow in the normal physiological state. Pathological stimulation of the eicosanoid metabolite cascade may contribute to the development of vasospasm after SAH.…”